CAR-T cell therapy works well in blood cancers, but faces difficulty in solid tumours due to antigen heterogeneity
Tumour cells previously thought “undetectable” actually express very low levels of CD70 protein
This low expression is not absence, but a hidden signal missed by conventional CAR-T cells
Scientists developed a HIT (HLA-independent T-cell) receptor to detect these faint signals
HIT receptor links detection directly to the natural activation pathway of T-cells
In experimental models, HIT-based T-cells showed complete and long-lasting tumour removal
Detailed Insights:
Antigen heterogeneity in solid tumors allows some cells to evade detection by CAR-T cells, leading to cancer regrowth.
The enzyme EZH2 suppresses the gene for CD70, reducing its production and making cells undetectable to current immune therapies.
The HIT receptor bypasses the HLA system, enabling it to detect antigens at much lower densities than synthetic CAR-T cells.
Safety concerns about the HIT receptor reacting to normal cells were addressed by analyzing a single-cell atlas, which showed limited CD70 activity in vital organs.
Drug-tolerant persisters, which survive targeted therapies, can be addressed by the HIT receptor's ability to uncover and eliminate hidden cells.
Key Concepts Involved:
CAR-T Cell Therapy: Immunotherapy using engineered T-cells to identify and destroy cancer cells
Antigen Heterogeneity: Variation in protein expression across tumour cells, enabling immune evasion
HLA System: Cell-surface protein system that helps immune cells recognise targets
Pseudo-heterogeneity: Apparent absence of antigen due to extremely low expression levels